Our understanding of the neurobiology of the Platyhelminthes has come in large part from free-living turbellarians. In addition to providing considerable information about the capabilities of the rudimentary nervous system present in all members of the phylum, turbellarians have provided the most definitive information about the variety of ion channels present in the membranes of neurones and muscle cells, and about the physiology and pharmacology of those channels. Furthermore, preparations of single, viable muscle cells have provided some of the most conclusive evidence about the variety of transmitters present, and the types of response they evoke. Here, we review what is known about the physiology and pharmacology of the turbellarian neuromuscular system. Particular attention is given to the triclad flatworm Bdelloura Candida, the best studied species in this respect, but other species are included where relevant.

A protocol for dissociating single muscle fibres from intact flatworms was developed. Muscle fragments of various sizes were obtained, many with their cell bodies, or myocytons, intact. Many of the fibres were spontaneously contractile, and they and others contracted in response to applications of transmitter candidates, activators of protein kinase C and the anthelmintic praziquantel. The responses were all similar to those evoked in strips of tissue. Voltage clamp recordings from the isolated muscle fibres revealed that they possess an inward Ca2+ current and 3 separate K+ currents. These results indicate that muscle fibres in Bdelloura bear receptors for neurotransmitters and that preparations of dispersed muscle fibres can be used for studying the basic physiological and pharmacological properties of platyhelminth muscle.

Ascorbate modulates IK(V) of ON-type mixed rod/cone bipolar cells (Mb) in the goldfish retinal slice through a dopamine D1/G-protein/PKA-coupled mechanism. We investigated the effects of dopamine depletion with intraocular injections of 6-OHDA on IK(V) and its modulation by ascorbate over 1–7 weeks following 6-OHDA treatment. Dopamine depletion was verified by tyrosine hydroxylase immunocytochemistry. Slices were perfused in a saline containing 200 μM sodium ascorbate. One-second puffs of ascorbate-free saline (zero [AA]o), delivered through a 2–3 μm diameter pipette, were directed at the bipolar cells. IK(V) was recorded by conventional whole-cell patch-clamp methods. In normal retinas, puffs of zero [AA]o caused a rapid (<100 ms) suppression of IK(V) of about 50% that lasted for several minutes. This effect was blocked by 1 μM SCH23390 and was unaffected by 2 mM Co2+ or 5 μM spiperone. 6-OHDA treatment resulted in major effects. First, IK(V) was reduced by ∼50% for weeks 1–6, recovering to a 20% reduction by week 7. Second, puffs of zero [AA]o enhanced IK(V) rather than suppressed it. The enhancement was blocked by SCH23390 and the PKA inhibitor, Wiptide, but was insensitive to spiperone. Third, all parts of the Mb bipolar cell (except for the axon) were sensitive to puffs of zero [AA]o in both normal and 6-OHDA-treated retinas. Fourth, bath application of 20 μM dopamine restored the amplitude of IK(V) but did not reverse the effects of puffed zero [AA]o. IK(V) was fit by two exponentials; all of the effects on IK(V) were on the amplitude of the components and not on the time constants. Chronic dopamine depletion caused reversible changes in the properties of K+ channels underlying IK(V), as well as a long-term change in the intracellular coupling mechanisms between D1-receptor activation and the modulation of IK(V).

Müller cells are highly permeable to potassium ions and play a major role in maintaining potassium homeostasis in the vertebrate retina during light-evoked neuronal activity. Potassium fluxes across the Müller cell's membrane are believed to underlie the light-evoked responses of these cells. We studied the potassium currents of turtle Müller cells in the retinal slice and in dissociated cell preparations and their role in the genesis of the light-evoked responses of these cells. In either preparation, the I–V curve, measured under voltage-clamp conditions, consisted of inward and outward currents. A mixture of cesium ions, TEA, and 4-AP blocked the inward current but had no effect on the outward current. Extracellular cesium ions alone blocked the inward current but exerted no effect on the photoresponses. Extracellular barium ions blocked both inward and outward currents, induced substantial depolarization, and augmented the light-evoked responses, especially the OFF component. Exposing isolated Müller cells to a high potassium concentration did not cause any current or voltage responses when barium ions were present. In contrast, application of glutamate in the presence of barium ions induced a small inward current that was associated with a substantially augmented depolarizing wave relative to that observed under control conditions. This observation suggests a role for an electrogenic glutamate transporter in generating the OFF component of the turtle Müller cell photoresponse.